Ca 2+ Signals and Neuronal Death in Brain Ischemia
| Autor: | Pierluigi Nicotera, Daniele Bano |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
Pathology
medicine.medical_specialty Programmed cell death chemistry.chemical_element Calcium Neuroprotection Calcium in biology Brain Ischemia Cellular ion homeostasis Animals Humans Medicine Calcium Signaling Calcium signaling Neurons Advanced and Specialized Nursing Cell Death biology business.industry Glutamate receptor Calpain Cell biology chemistry biology.protein Neurology (clinical) Cardiology and Cardiovascular Medicine business |
| Zdroj: | Stroke. 38:674-676 |
| ISSN: | 1524-4628 0039-2499 |
| Popis: | Although Ca 2+ signals are necessary for cell communication and survival, abnormal cellular Ca 2+ load can trigger different cell death programs. Ca 2+ mediates cell death by activating proteases (ie, calpains), by reinforcing signals leading to caspase activation or by triggering other catabolic processes mediated by lipases and nucleases. Failure in the clearance of excitatory amino acid is a critical determinant of neuronal loss in the ischemic brain. Glutamate activates glutamate-ionotropic receptors at synaptic and extra-synaptic sites, causing prolonged neuronal depolarization and triggering deregulation of cellular ion homeostasis, mainly intracellular calcium and sodium. The mechanisms leading to the sustained calcium deregulation in excitotoxic conditions are only in part elucidated. Recently, we have shown that calpains mediate the inhibition of calcium efflux in primary dissociated neurons challenged with excitotoxic glutamate concentrations. Calpains cleave the sodium-calcium exchanger (NCX) and inhibit its capability to remove calcium accumulated as a consequence of the excitotoxic stimulus. Our findings highlight the link between calcium-dependent proteases, calcium overload and neuronal degeneration after an excitotoxic insult. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|